Platelets and coagulation in thrombus formation: aberrations in the Scott syndrome

Thromb Res. 2016 May:141 Suppl 2:S12-6. doi: 10.1016/S0049-3848(16)30355-3.

Abstract

Platelets play key roles in thrombosis and hemostasis by forming aggregates and providing a procoagulant surface, at which thrombin is generated and fibrin fibers are formed. Here we present an overview of the different mechanisms how platelets orchestrate coagulation processes in thrombus formation in thrombosis and hemostasis. Parts of these are via Ca(2+)-dependent activation responses, leading to phosphatidylserine exposure; swelling to form balloons with increased binding of coagulation factors; and calpain-mediated integrin αIIbβ3 cleavage and inactivation. Other mechanisms are secretion of (anti) coagulation factors, and αIIbβ3-mediated thrombus retraction, and clot retraction. In a thrombus, coagulation factors are found at both platelets and fibrin fibers. Many of the procoagulant platelet activities are altered in the Scott syndrome.

Keywords: Bleeding; phosphatidylserine; platelet; thrombin; thrombus.

Publication types

  • Review

MeSH terms

  • Animals
  • Blood Coagulation
  • Blood Coagulation Disorders / blood
  • Blood Coagulation Disorders / metabolism
  • Blood Coagulation Disorders / pathology*
  • Blood Platelets / metabolism
  • Blood Platelets / pathology*
  • Hemostasis*
  • Humans
  • Platelet Activation
  • Thrombin / metabolism
  • Thrombosis / blood
  • Thrombosis / metabolism
  • Thrombosis / pathology*

Substances

  • Thrombin

Supplementary concepts

  • Scott Syndrome